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Article

Toll-like Receptor Signaling Inhibitory Peptide Improves Inflammation in Animal Model and Human Systemic Lupus Erythematosus

1
Department of Rheumatology, Ajou University School of Medicine, 164 Worldcup-ro, Suwon 16499, Korea
2
Department of Molecular Science and Technology, Ajou University, 164 Worldcup-ro, Suwon 16499, Korea
*
Author to whom correspondence should be addressed.
Academic Editor: Arcangelo Liso
Int. J. Mol. Sci. 2021, 22(23), 12764; https://doi.org/10.3390/ijms222312764
Received: 28 October 2021 / Revised: 19 November 2021 / Accepted: 22 November 2021 / Published: 25 November 2021
Toll-like receptors (TLRs) play a major role in the innate immune system. Several studies have shown the regulatory effects of TLR-mediated pathways on immune and inflammatory diseases. Dysregulated functions of TLRs within the endosomal compartment, including TLR7/9 trafficking, may cause systemic lupus erythematosus (SLE). TLR signaling pathways are fine-tuned by Toll/interleukin-1 receptor (TIR) domain-containing adapters, leading to interferon (IFN)-α production. This study describes a TLR inhibitor peptide 1 (TIP1) that primarily suppresses the downstream signaling mediated by TIR domain-containing adapters in an animal model of lupus and patients with SLE. The expression of most downstream proteins of the TLR7/9/myeloid differentiation factor 88 (MyD88)/IFN regulatory factor 7 signaling was downregulated in major tissues such as the kidney, spleen, and lymph nodes of treated mice. Furthermore, the pathological analysis of the kidney tissue confirmed that TIP1 could improve inflammation in MRL/lpr mice. TIP1 treatment downregulated many downstream proteins associated with TLR signaling, such as MyD88, interleukin-1 receptor-associated kinase, tumor necrosis factor receptor-associated factor 6, and IFN-α, in the peripheral blood mononuclear cells of patients with SLE. In conclusion, our data suggest that TIP1 can serve as a potential candidate for the treatment of SLE. View Full-Text
Keywords: lupus erythematosus; systemic; Toll-like receptors; mice; inbred MRL/lpr lupus erythematosus; systemic; Toll-like receptors; mice; inbred MRL/lpr
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MDPI and ACS Style

Baek, W.-Y.; Choi, Y.-S.; Lee, S.-W.; Son, I.-O.; Jeon, K.-W.; Choi, S.-D.; Suh, C.-H. Toll-like Receptor Signaling Inhibitory Peptide Improves Inflammation in Animal Model and Human Systemic Lupus Erythematosus. Int. J. Mol. Sci. 2021, 22, 12764. https://doi.org/10.3390/ijms222312764

AMA Style

Baek W-Y, Choi Y-S, Lee S-W, Son I-O, Jeon K-W, Choi S-D, Suh C-H. Toll-like Receptor Signaling Inhibitory Peptide Improves Inflammation in Animal Model and Human Systemic Lupus Erythematosus. International Journal of Molecular Sciences. 2021; 22(23):12764. https://doi.org/10.3390/ijms222312764

Chicago/Turabian Style

Baek, Wook-Young, Yang-Seon Choi, Sang-Won Lee, In-Ok Son, Ki-Woong Jeon, Sang-Dun Choi, and Chang-Hee Suh. 2021. "Toll-like Receptor Signaling Inhibitory Peptide Improves Inflammation in Animal Model and Human Systemic Lupus Erythematosus" International Journal of Molecular Sciences 22, no. 23: 12764. https://doi.org/10.3390/ijms222312764

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